American Journal of Emergency Medicine 32 (2014) 286.e5–286.e9
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Case Report
Stress-related cardiomyopathy, ventricular dysfunction, artery thrombosis: a hidden pheochromocytoma Abstract Clinical presentation of pheochromocytoma can vary, and it can sometimes mimic other diseases. Some patients with pheochromocytoma may have atypical presentations, such as clinical features consistent with an acute coronary syndrome, that only later suggest a classical picture of stress-related cardiomyopathy. To our best knowledge, pheochromocytoma has been incidentally revealed in a few cases of catecholamine-induced cardiomyopathy and in only 1 case of peripheral arterial thrombosis. This is the first case of pheochromocytoma revealed after left ventricular dysfunction caused by stress-related cardiomyopathy associated with inferior limb artery thrombosis in a patient with a complex cardiovascular history. We report a case of a 63-year-old white woman with catecholamine-induced cardiomyopathy, mimicking acute coronary syndromes (ACSs), left ventricular dysfunction, peripheral arterial thrombosis, and an unrevealed pheochromocytoma incidentally diagnosed. This case highlights the complexity of managing patients with atypical clinical presentation and multitude of symptoms mimicking other diseases. Pheocromocytoma remains often undiagnosed, and atypical presentation of stress-related cardiomyopathy could suggest a hidden pheochromocytoma, especially in a patient with an extensive cardiovascular history.
A smoker, obese, 63-year-old white woman with a medical history of hypertension, dyslipidemia, and previous ischemic stroke was referred to our emergency department with resting dyspnea and peripheral coldness. The patient presented with precordial pain, which started 24 hours before and lasted 30 minutes. Physical examination revealed a blood pressure of 120/75 mm Hg, heart rate of 100 beats/min, and oxygen saturation of 94%, as well as normal heart sounds and fine crackles over both lung bases. Chest x-ray showed typical findings of an acute pulmonary edema. Electrocardiogram (ECG) showed ST-segment elevation in V2 to V4 and T-wave inversion in V2 to V6 precordial leads, suggesting a subacute myocardial infarction (Fig. 1). On admission to intensive care unit, echocardiography showed akinesia of all mid and apical segments with normal basal contraction and systolic function impairment (ejection fraction, 35%), typically consistent with takotsubo cardiomyopathy (TTC). Furthermore, she admitted to have a recent history of moderate psychological distress. Laboratory findings are shown in Table 1A. A coronary angiography with a right radial approach showed normal coronary arteries (Fig. 2A, B). Left ventriculography showed an apical akinesia of the anterior wall with enhanced contractility of basal segments (Fig. 2C, D). Few hours later, the patient complained of right leg pain and paresthesia. The leg appeared cold and pale, with lack of tibial and
Fig. 1. On admission, 12-lead ECG showed segment elevation in V2 to V4 and T-wave inversion in V2 - V6 precordial leads. 0735-6757/$ – see front matter © 2014 Elsevier Inc. All rights reserved.
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A. Battimelli et al. / American Journal of Emergency Medicine 32 (2014) 286.e5–286.e9
Table 1 Laboratory values of the patient at hospitalization (A) and after CT (B) Values
Reference ranges
Hemoglobine Red blood cells Hematocrit White blood cells Platelets Blood glucose Creatinine Troponin Myoglobin Creatine kinase–MB Lactate dehydrogenase Brain natriuretic peptide
16.1 g/dL 6.18 × 106/μL 50.20% 22.26 × 103/μL 433 × 103/μL 150 mg/dL 2 mg/dL 24.30 ng/mL 5668 ng/mL N300 ng/mL 1820 U/L 2917 U/L
12-15 g/dL 3.8-5.0 × 106/μL 35 %-48 % 4.5-10.00 × 103/μL 150-400 × 103/μL 60-110 mg/dL 0.7-1.3 mg/dL 0-0.05 ng/mL 0-116 ng/mL 0-3.8 ng/mL 313-618 U/L 0-160 U/L
Plasma metanephrine Plasma normetanephrine Plasma cortisol (at 6 o'clock) Urinary cortisol
14.3 nmol/L 24.1 nmol/L 32.7 μg/dL 1373 μg/24 h
b 0.49 nmol/L b 0.89 nmol/L 8 to 23 μg/dL 50 to 200 μg/24 h
A
B
pedal pulses. Then, a computed tomography angiography (angioCT) was performed, revealing an abrupt interruption of posterior right tibial artery and a significant reduction of left posterior tibial artery flow (Fig. 3). Incidentally, a voluminous (7 × 6 × 5 cm) and inhomogeneous left adrenal gland mass was revealed (Fig. 4). These results indicated a percutaneous transluminal angioplasty to restore the perfusion of the right leg (Fig. 5). Right posterior tibial lesion was treated, achieving a suboptimal reperfusion. Moreover, the findings of angioCT led to suspect a pheochromocytoma and imposed more specific laboratory reports, which revealed significantly elevated levels of plasma metanephrine and normetanephrine, plasma cortisol, and urinary cortisol (Table 1B). Three weeks later, elective surgery was performed.
Histopathologic findings of the removed lesion (Fig. 6) confirmed that the tumor was a pheochromocytoma. Many patients with clinical features consistent with an ACS after a diagnostic workup revealed other diseases. Atypical presentations often delay correct diagnosis or lead to misdiagnosis. In 1.5% to 2.2% of patients presenting with symptoms that initially appear to be an ACS [1], TTC is revealed. Our patient presented with many hallmarks of TTC, and until pheochromocytoma was found, the 4 “Mayo Clinic” diagnostic criteria [2] required for the diagnosis of TTC were satisfied (Table 2). The literature indicates that the pathophysiology of TTC and pheochromocytoma-related cardiomyopathy is similar and mediated by catecholamines [3]. The left ventricular wall motion abnormality in patients with pheochromocytoma crisis is generally global, although apical-sparing and TTC-like wall motion abnormalities have been reported [4,5]. Thus, Bybee and Prasad [2] suggested a modified version of the diagnostic criteria for TTC (Table 3), in which the lack of proven pheochromocytoma does not appear. This tumor is probably underdiagnosed and is often missed. Incidentally, in our patient, pheochromocytoma was diagnosed with angioCT performed for acute right lower limb ischemia occurred during hospitalization. Catecholamine-induced cardiomyopathy has been ascertained in some cases of pheochromocytoma, and there are some reports of pheochromocytomas presenting as ACS [6]. In our case, clinical presentation was complex: ST-segment elevation myocardial infarction, stress-related cardiomyopathy, left ventricular dysfunction, and peripheral arterial thrombosis. During hospitalization, the patient showed thrombophilic diathesis, with the presence of right leg arterial thrombosis. The possibility of embolization after diagnostic coronary angiography was excluded because of use of transradial approach for cardiac catheterization. Thrombotic events have been reported rarely in patients with pheochromocytoma, and the exact mechanism of thrombosis is unclear [7].
Fig. 2. Diagnostic coronary angiography: left coronary artery with branches to left anterior descending artery and left circumflex artery (normal [A]) and right coronary artery (normal [B]). Left ventriculography (in diastole [C] and in systole [D]) showing systolic dysfunction of the left ventricular apex and midventricle, with hyperkinesis of the basal left ventricular segments.
A. Battimelli et al. / American Journal of Emergency Medicine 32 (2014) 286.e5–286.e9
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Fig. 3. Computed tomography angiography: reconstruction of arterial vascularization of the left and right legs. A, Left leg: arterial vascularization is normal. B, Right leg: anterior right tibial artery is normal, but there is an abrupt interruption of posterior right tibial artery.
Certainly, our patient could be included in the setting of a hypercoagulative state, as in all patients with cancer. It is often a result of inflammatory cytokines and procoagulants secreted by tumor cells [8]. This may predispose patient to form thrombi in low flow areas. Furthermore, our patient admitted to have ischemic stroke 5 years before; her aorta was atherosclerotic and contained multiple areas of friable plaques. Similar to reports in the literature [9], our patient also had an increased white blood cell count and platelet count, in addition to an increased red blood cell count. These features suggest a paraneoplastic syndrome that might have contributed to the onset of thrombosis in our patient. This case highlights the complexity of managing patients with atypical clinical presentation of cardiac and vascular diseases and the possibility that a multitude of symptoms mimic other disease. We conclude that any atypical presentation of stress-related cardiomyopathy could suggest an unrevealed pheochromocytoma, and even if the priority is to treat an acute event, in the second time, noninvasive approaches should be performed, especially in a patient with an extensive cardiovascular history.
Anna Battimelli MD Maria Vincenza Polito MD Marco Di Maio MD Susanna Poto MD Luciana Pierro MD School of Medicine Department of Medicine and Surgery University of Salerno Salerno, Italy E-mail addresses: [email protected] [email protected] [email protected] [email protected] [email protected] Domenico Caggiano MD Department of Medicine, University hospital “S. Giovanni Di Dio e Ruggi D' Aragona” Salerno, Italy E-mail address: [email protected]
Fig. 4. Computed tomographic scan of the abdomen: a voluminous and inhomogeneous left adrenal gland mass that showed avid contrast enhancement and slow contrast washout and a central colliquative necrotic area.
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A. Battimelli et al. / American Journal of Emergency Medicine 32 (2014) 286.e5–286.e9
Fig. 5. Percutaneous transluminal angioplasty (PTA) of the right leg. A and B, before PTA, anterior tibial artery is normal, and there is a severe obstruction of posterior tibial artery. C, stent placement in posterior tibial artery. D, after PTA and stenting, angiogram shows reperfusion of treated vessel with persistence of proximal stenosis.
Federico Piscione MD School of Medicine, Department of Medicine and Surgery University of Salerno Salerno, Italy E-mail address: [email protected] http://dx.doi.org/10.1016/j.ajem.2013.09.034 References [1] Kurowski V, Kaiser A, von Hof K, et al. Apical and mid ventricular transient left ventricular dysfunction syndrome (tako-tsubo cardio-myopathy): frequency, mechanisms, and prognosis. Chest 2007;132:809–16. [2] Bybee KA, Prasad A. Stress-related cardiomyopathy syndromes. Circulation 2008;118:397–409.
[3] Wittstein IS, Thiemann DR, Lima JA, et al. Neurohumoral features of myocardial stunning due to emotional stress. N Engl J Med 2005;352:539–48. [4] Yoshinaga K, Torii H, Tahara M. A serial echocardiographic observation of acute heart injury associated with pheochromocytoma crisis. Int J Cardiol 1998;66: 199–202. [5] Takizawa M, Kobayakawa N, Uozumi H, et al. A case of transient left ventricular ballooning with pheochromocytoma, supporting pathogenetic role of catecholamines in stress- induced cardiomyopathy or takotsubo cardiomyopathy. Int J Cardiol 2007;114:e15–7. [6] Agarwal V, Kant G, Hans N, et al. Takotsubo-like cardiomyopathy in pheochromocytoma. Int J Cardiol 2011;153:241–8. [7] Zhou W, Ding SF. Concurrent pheochromocytoma, ventricular tachycardia, left ventricular thrombus, and systemic embolization. Intern Med 2009;48:1015–9. [8] Zwicker JI, Furie BC, Furie B. Cancer-associated thrombosis. Crit Rev Oncol Hematol 2007;62:126–36. [9] Zelinka T, Petrâk O, Strauch B, et al. Elevated inflammation markers in pheochromocytoma compared to other forms of hypertension. Neuroimmunomodulation 2007;14:57–64.
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Fig. 6. Microscopic and immunohistochemical findings. A, zellballen architecture is the most common architectural pattern of pheochromocytoma. The balls of cells are supported by a rich vascular plexus and a dendritic to spindle cell sustentacular meshwork. The cytoplasm of the neoplastic cells has a finely granular character. B, in the upper left normal cortex of the adrenal gland and in the lower right neoplastic cells of pheochromocytoma, pleomorphism and bizarre hyperchromatic nuclei are present. The diagnostic hallmarks are neurosecretory granules containing epinephrine or norepinephrine. C, CD56 is one of the neuroendocrine-type markers that is positive in pheochromocytoma, such as in our case. D, pheochromocytes react strongly and diffusely with synaptophysin, a neuroendocrine marker typically positive in pheochromocytoma.
Table 2 Mayo Clinic diagnostic criteria (1) Transient left ventricular wall motion abnormalities involving the apical and/ or midventricular myocardial segments with wall motion abnormalities extending beyond a single epicardial coronary artery distribution (2) Absence of obstructive epicardial coronary artery disease that could be responsible for the observed wall motion abnormality (3) ECG abnormalities such as transient ST-segment elevation and/or diffuse Twave inversion associated with a slight troponin elevation (4) The lack of proven pheochromocytoma and myocarditis
Table 3 Modified version for diagnosis of tako-tsubo cardiomyopathy—Bybee and Prasad [2] (1) Transient left ventricular wall motion abnormalities involving the apical and/ or midventricular myocardial segments with wall motion abnormalities extending beyond a single epicardial coronary distribution (2) Absence of obstructive epicardial coronary artery disease or angiographic evidence of acute plaque rupture that could be responsible for the observed wall motion abnormality (3) New ECG abnormalities such as transient ST-segment elevation and/or diffuse T-wave inversions or troponin elevation.
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Case Report
Stress-related cardiomyopathy, ventricular dysfunction, artery thrombosis: a hidden pheochromocytoma Abstract Clinical presentation of pheochromocytoma can vary, and it can sometimes mimic other diseases. Some patients with pheochromocytoma may have atypical presentations, such as clinical features consistent with an acute coronary syndrome, that only later suggest a classical picture of stress-related cardiomyopathy. To our best knowledge, pheochromocytoma has been incidentally revealed in a few cases of catecholamine-induced cardiomyopathy and in only 1 case of peripheral arterial thrombosis. This is the first case of pheochromocytoma revealed after left ventricular dysfunction caused by stress-related cardiomyopathy associated with inferior limb artery thrombosis in a patient with a complex cardiovascular history. We report a case of a 63-year-old white woman with catecholamine-induced cardiomyopathy, mimicking acute coronary syndromes (ACSs), left ventricular dysfunction, peripheral arterial thrombosis, and an unrevealed pheochromocytoma incidentally diagnosed. This case highlights the complexity of managing patients with atypical clinical presentation and multitude of symptoms mimicking other diseases. Pheocromocytoma remains often undiagnosed, and atypical presentation of stress-related cardiomyopathy could suggest a hidden pheochromocytoma, especially in a patient with an extensive cardiovascular history.
A smoker, obese, 63-year-old white woman with a medical history of hypertension, dyslipidemia, and previous ischemic stroke was referred to our emergency department with resting dyspnea and peripheral coldness. The patient presented with precordial pain, which started 24 hours before and lasted 30 minutes. Physical examination revealed a blood pressure of 120/75 mm Hg, heart rate of 100 beats/min, and oxygen saturation of 94%, as well as normal heart sounds and fine crackles over both lung bases. Chest x-ray showed typical findings of an acute pulmonary edema. Electrocardiogram (ECG) showed ST-segment elevation in V2 to V4 and T-wave inversion in V2 to V6 precordial leads, suggesting a subacute myocardial infarction (Fig. 1). On admission to intensive care unit, echocardiography showed akinesia of all mid and apical segments with normal basal contraction and systolic function impairment (ejection fraction, 35%), typically consistent with takotsubo cardiomyopathy (TTC). Furthermore, she admitted to have a recent history of moderate psychological distress. Laboratory findings are shown in Table 1A. A coronary angiography with a right radial approach showed normal coronary arteries (Fig. 2A, B). Left ventriculography showed an apical akinesia of the anterior wall with enhanced contractility of basal segments (Fig. 2C, D). Few hours later, the patient complained of right leg pain and paresthesia. The leg appeared cold and pale, with lack of tibial and
Fig. 1. On admission, 12-lead ECG showed segment elevation in V2 to V4 and T-wave inversion in V2 - V6 precordial leads. 0735-6757/$ – see front matter © 2014 Elsevier Inc. All rights reserved.
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A. Battimelli et al. / American Journal of Emergency Medicine 32 (2014) 286.e5–286.e9
Table 1 Laboratory values of the patient at hospitalization (A) and after CT (B) Values
Reference ranges
Hemoglobine Red blood cells Hematocrit White blood cells Platelets Blood glucose Creatinine Troponin Myoglobin Creatine kinase–MB Lactate dehydrogenase Brain natriuretic peptide
16.1 g/dL 6.18 × 106/μL 50.20% 22.26 × 103/μL 433 × 103/μL 150 mg/dL 2 mg/dL 24.30 ng/mL 5668 ng/mL N300 ng/mL 1820 U/L 2917 U/L
12-15 g/dL 3.8-5.0 × 106/μL 35 %-48 % 4.5-10.00 × 103/μL 150-400 × 103/μL 60-110 mg/dL 0.7-1.3 mg/dL 0-0.05 ng/mL 0-116 ng/mL 0-3.8 ng/mL 313-618 U/L 0-160 U/L
Plasma metanephrine Plasma normetanephrine Plasma cortisol (at 6 o'clock) Urinary cortisol
14.3 nmol/L 24.1 nmol/L 32.7 μg/dL 1373 μg/24 h
b 0.49 nmol/L b 0.89 nmol/L 8 to 23 μg/dL 50 to 200 μg/24 h
A
B
pedal pulses. Then, a computed tomography angiography (angioCT) was performed, revealing an abrupt interruption of posterior right tibial artery and a significant reduction of left posterior tibial artery flow (Fig. 3). Incidentally, a voluminous (7 × 6 × 5 cm) and inhomogeneous left adrenal gland mass was revealed (Fig. 4). These results indicated a percutaneous transluminal angioplasty to restore the perfusion of the right leg (Fig. 5). Right posterior tibial lesion was treated, achieving a suboptimal reperfusion. Moreover, the findings of angioCT led to suspect a pheochromocytoma and imposed more specific laboratory reports, which revealed significantly elevated levels of plasma metanephrine and normetanephrine, plasma cortisol, and urinary cortisol (Table 1B). Three weeks later, elective surgery was performed.
Histopathologic findings of the removed lesion (Fig. 6) confirmed that the tumor was a pheochromocytoma. Many patients with clinical features consistent with an ACS after a diagnostic workup revealed other diseases. Atypical presentations often delay correct diagnosis or lead to misdiagnosis. In 1.5% to 2.2% of patients presenting with symptoms that initially appear to be an ACS [1], TTC is revealed. Our patient presented with many hallmarks of TTC, and until pheochromocytoma was found, the 4 “Mayo Clinic” diagnostic criteria [2] required for the diagnosis of TTC were satisfied (Table 2). The literature indicates that the pathophysiology of TTC and pheochromocytoma-related cardiomyopathy is similar and mediated by catecholamines [3]. The left ventricular wall motion abnormality in patients with pheochromocytoma crisis is generally global, although apical-sparing and TTC-like wall motion abnormalities have been reported [4,5]. Thus, Bybee and Prasad [2] suggested a modified version of the diagnostic criteria for TTC (Table 3), in which the lack of proven pheochromocytoma does not appear. This tumor is probably underdiagnosed and is often missed. Incidentally, in our patient, pheochromocytoma was diagnosed with angioCT performed for acute right lower limb ischemia occurred during hospitalization. Catecholamine-induced cardiomyopathy has been ascertained in some cases of pheochromocytoma, and there are some reports of pheochromocytomas presenting as ACS [6]. In our case, clinical presentation was complex: ST-segment elevation myocardial infarction, stress-related cardiomyopathy, left ventricular dysfunction, and peripheral arterial thrombosis. During hospitalization, the patient showed thrombophilic diathesis, with the presence of right leg arterial thrombosis. The possibility of embolization after diagnostic coronary angiography was excluded because of use of transradial approach for cardiac catheterization. Thrombotic events have been reported rarely in patients with pheochromocytoma, and the exact mechanism of thrombosis is unclear [7].
Fig. 2. Diagnostic coronary angiography: left coronary artery with branches to left anterior descending artery and left circumflex artery (normal [A]) and right coronary artery (normal [B]). Left ventriculography (in diastole [C] and in systole [D]) showing systolic dysfunction of the left ventricular apex and midventricle, with hyperkinesis of the basal left ventricular segments.
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Fig. 3. Computed tomography angiography: reconstruction of arterial vascularization of the left and right legs. A, Left leg: arterial vascularization is normal. B, Right leg: anterior right tibial artery is normal, but there is an abrupt interruption of posterior right tibial artery.
Certainly, our patient could be included in the setting of a hypercoagulative state, as in all patients with cancer. It is often a result of inflammatory cytokines and procoagulants secreted by tumor cells [8]. This may predispose patient to form thrombi in low flow areas. Furthermore, our patient admitted to have ischemic stroke 5 years before; her aorta was atherosclerotic and contained multiple areas of friable plaques. Similar to reports in the literature [9], our patient also had an increased white blood cell count and platelet count, in addition to an increased red blood cell count. These features suggest a paraneoplastic syndrome that might have contributed to the onset of thrombosis in our patient. This case highlights the complexity of managing patients with atypical clinical presentation of cardiac and vascular diseases and the possibility that a multitude of symptoms mimic other disease. We conclude that any atypical presentation of stress-related cardiomyopathy could suggest an unrevealed pheochromocytoma, and even if the priority is to treat an acute event, in the second time, noninvasive approaches should be performed, especially in a patient with an extensive cardiovascular history.
Anna Battimelli MD Maria Vincenza Polito MD Marco Di Maio MD Susanna Poto MD Luciana Pierro MD School of Medicine Department of Medicine and Surgery University of Salerno Salerno, Italy E-mail addresses: [email protected] [email protected] [email protected] [email protected] [email protected] Domenico Caggiano MD Department of Medicine, University hospital “S. Giovanni Di Dio e Ruggi D' Aragona” Salerno, Italy E-mail address: [email protected]
Fig. 4. Computed tomographic scan of the abdomen: a voluminous and inhomogeneous left adrenal gland mass that showed avid contrast enhancement and slow contrast washout and a central colliquative necrotic area.
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A. Battimelli et al. / American Journal of Emergency Medicine 32 (2014) 286.e5–286.e9
Fig. 5. Percutaneous transluminal angioplasty (PTA) of the right leg. A and B, before PTA, anterior tibial artery is normal, and there is a severe obstruction of posterior tibial artery. C, stent placement in posterior tibial artery. D, after PTA and stenting, angiogram shows reperfusion of treated vessel with persistence of proximal stenosis.
Federico Piscione MD School of Medicine, Department of Medicine and Surgery University of Salerno Salerno, Italy E-mail address: [email protected] http://dx.doi.org/10.1016/j.ajem.2013.09.034 References [1] Kurowski V, Kaiser A, von Hof K, et al. Apical and mid ventricular transient left ventricular dysfunction syndrome (tako-tsubo cardio-myopathy): frequency, mechanisms, and prognosis. Chest 2007;132:809–16. [2] Bybee KA, Prasad A. Stress-related cardiomyopathy syndromes. Circulation 2008;118:397–409.
[3] Wittstein IS, Thiemann DR, Lima JA, et al. Neurohumoral features of myocardial stunning due to emotional stress. N Engl J Med 2005;352:539–48. [4] Yoshinaga K, Torii H, Tahara M. A serial echocardiographic observation of acute heart injury associated with pheochromocytoma crisis. Int J Cardiol 1998;66: 199–202. [5] Takizawa M, Kobayakawa N, Uozumi H, et al. A case of transient left ventricular ballooning with pheochromocytoma, supporting pathogenetic role of catecholamines in stress- induced cardiomyopathy or takotsubo cardiomyopathy. Int J Cardiol 2007;114:e15–7. [6] Agarwal V, Kant G, Hans N, et al. Takotsubo-like cardiomyopathy in pheochromocytoma. Int J Cardiol 2011;153:241–8. [7] Zhou W, Ding SF. Concurrent pheochromocytoma, ventricular tachycardia, left ventricular thrombus, and systemic embolization. Intern Med 2009;48:1015–9. [8] Zwicker JI, Furie BC, Furie B. Cancer-associated thrombosis. Crit Rev Oncol Hematol 2007;62:126–36. [9] Zelinka T, Petrâk O, Strauch B, et al. Elevated inflammation markers in pheochromocytoma compared to other forms of hypertension. Neuroimmunomodulation 2007;14:57–64.
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Fig. 6. Microscopic and immunohistochemical findings. A, zellballen architecture is the most common architectural pattern of pheochromocytoma. The balls of cells are supported by a rich vascular plexus and a dendritic to spindle cell sustentacular meshwork. The cytoplasm of the neoplastic cells has a finely granular character. B, in the upper left normal cortex of the adrenal gland and in the lower right neoplastic cells of pheochromocytoma, pleomorphism and bizarre hyperchromatic nuclei are present. The diagnostic hallmarks are neurosecretory granules containing epinephrine or norepinephrine. C, CD56 is one of the neuroendocrine-type markers that is positive in pheochromocytoma, such as in our case. D, pheochromocytes react strongly and diffusely with synaptophysin, a neuroendocrine marker typically positive in pheochromocytoma.
Table 2 Mayo Clinic diagnostic criteria (1) Transient left ventricular wall motion abnormalities involving the apical and/ or midventricular myocardial segments with wall motion abnormalities extending beyond a single epicardial coronary artery distribution (2) Absence of obstructive epicardial coronary artery disease that could be responsible for the observed wall motion abnormality (3) ECG abnormalities such as transient ST-segment elevation and/or diffuse Twave inversion associated with a slight troponin elevation (4) The lack of proven pheochromocytoma and myocarditis
Table 3 Modified version for diagnosis of tako-tsubo cardiomyopathy—Bybee and Prasad [2] (1) Transient left ventricular wall motion abnormalities involving the apical and/ or midventricular myocardial segments with wall motion abnormalities extending beyond a single epicardial coronary distribution (2) Absence of obstructive epicardial coronary artery disease or angiographic evidence of acute plaque rupture that could be responsible for the observed wall motion abnormality (3) New ECG abnormalities such as transient ST-segment elevation and/or diffuse T-wave inversions or troponin elevation.
